Evidence map›Paper›PMID 26667175›Full record

ArticleMolecular & cellular proteomics : MCP2016

Targeted Proteomics Identifies Paraoxonase/Arylesterase 1 (PON1) and Apolipoprotein Cs as Potential Risk Factors for Hypoalphalipoproteinemia in Diabetic Subjects Treated with Fenofibrate and Rosiglitazone.

Graziella E Ronsein, Gissette Reyes-Soffer, Yi He, Michael Oda, Henry Ginsberg, Jay W Heinecke

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
  2. Article
  3. The HDL Proteome Watch: Compilation of studies leads to new insights on HDL function.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2022
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Deepening our understanding of HDL proteome.Expert review of proteomics · 2019
    Review
  9. Article
  10. Article
  11. Review
  12. Time to ditch HDL-C as a measure of HDL function?Current opinion in lipidology · 2017
    Review
  13. Review
  14. Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Graziella E RonseinFrom the ‡Department of Medicine, University of Washington, Seattle, WA, 98109; ronsein@iq.usp.br.
Gissette Reyes-Soffer§ Columbia University College of Physicians and Surgeons, Department of Medicine, New York, NY 10032;
Yi HeFrom the ‡Department of Medicine, University of Washington, Seattle, WA, 98109;
Michael Oda¶Children's Hospital Oakland Research Institute, Oakland, CA 94609.
Henry Ginsberg§ Columbia University College of Physicians and Surgeons, Department of Medicine, New York, NY 10032;
Jay W HeineckeFrom the ‡Department of Medicine, University of Washington, Seattle, WA, 98109;
University of Washington · USColumbia University · US

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR024156 · NCRR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 2006 to 2011
$53.0M
Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 1986 to 2026
$41.4M
Clinical and Translational Science AwardUL1TR000040 · NCATS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 2012 to 2015
$26.2M
Role of Serum Amyloid A in Diabetic Vascular DiseaseP01HL092969 · NHLBI · UNIVERSITY OF WASHINGTON · PI VAISAR, TOMAS · 2008 to 2019
$23.5M
Assembly &Secretion Of Apo B Containing LipoproteinsR01HL055638 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 1996 to 2016
$5.9M
Quantitative Assessment of HDL FunctionR01HL112625 · NHLBI · UNIVERSITY OF WASHINGTON · PI HEINECKE, JAY W · 2012 to 2016
$2.1M
Pathways of fenofibrate effects on cardiovascular outcomes in ACCORDR01HL110418 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 2012 to 2014
$2.0M
Cardioprotective Mechanisms of HDLR01HL108897 · NHLBI · UNIVERSITY OF WASHINGTON · PI HEINECKE, JAY W · 2012 to 2015
$1.7M
APOC3, HDL Function and Cardiovascular Complications of T1DMDP3DK108209 · NIDDK · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E., HEINECKE, JAY W · 2015 to 2015
$1.6M
Postprandial Lipemia and Endothelial Function In ACCORDR01HL069190 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 2001 to 2004
$1.4M
NCATS NIH HHS UL1 TR000040NCRR NIH HHS UL1 RR024156NHLBI NIH HHS P01 HL092969NHLBI NIH HHS P01HL092969NHLBI NIH HHS R01 HL055638NHLBI NIH HHS R01 HL069190NHLBI NIH HHS R01 HL108897NHLBI NIH HHS R01HL108897NHLBI NIH HHS R01 HL110418NHLBI NIH HHS R01HL110418-03NHLBI NIH HHS R01 HL112625NHLBI NIH HHS R01HL112625NIDDK NIH HHS DP3 DK108209NIDDK NIH HHS P30 DK017047NIDDK NIH HHS P30DK017047
6 · The paper itself

Abstract

Low levels of high-density lipoprotein cholesterol (HDL-C) and high triglyceride levels contribute to the excess rate of cardiovascular events seen in subjects with type 2 diabetes. Fenofibrate treatment partially reverses dyslipidemia in these subjects. However, a paradoxical marked reduction in HDL-C and HDL's major protein, apolipoprotein A-I, is a complication of fenofibrate in combination with rosiglitazone, an insulin-sensitizing agent. Risk factors for this condition, termed hypoalphalipoproteinemia, have yet to be identified. Using a case-control study design with subjects enrolled in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial, we tested the hypothesis that alterations in HDL's protein cargo predispose diabetic subjects to fenofibrate/rosiglitazone-induced hypoalphalipoproteinemia. HDL was isolated from blood obtained from controls (no decreases or increase in HDL-C while receiving fenofibrate/rosiglitazone therapy) and cases (developed hypoalphalipoproteinemia after fenofibrate/rosiglitazone treatment) participating in the ACCORD study before they began fenofibrate/rosiglitazone treatment. HDL proteins were quantified by targeted parallel reaction monitoring (PRM) and selected reaction monitoring (SRM) with isotope dilution. This approach demonstrated marked increases in the relative concentrations of paraoxonase/arylesterase 1 (PON1), apolipoprotein C-II (APOC2), apolipoprotein C-I, and apolipoprotein H in the HDL of subjects who developed hypoalphalipoproteinemia. The case and control subjects did not differ significantly in baseline HDL-C levels or other traditional lipid risk factors. We used orthogonal biochemical techniques to confirm increased levels of PON1 and APOC2. Our observations suggest that an imbalance in HDL proteins predisposes diabetic subjects to develop hypoalphalipoproteinemia on fenofibrate/rosiglitazone therapy.

Indexed as

AgedApolipoprotein C-IIAryldialkylphosphataseCardiovascular DiseasesCase-Control StudiesDiabetes Mellitus, Type 2Drug Therapy, CombinationFemaleFenofibrateHumansHypoalphalipoproteinemiasHypoglycemic AgentsHypolipidemic AgentsLipoproteins, HDLMaleMiddle AgedApolipoprotein C-IIAryldialkylphosphataseFenofibrateHypoglycemic AgentsHypolipidemic AgentsLipoproteins, HDLPON1 protein, humanRosiglitazoneThiazolidinediones

Identifiers

PMID26667175
PMCPMC4813690
OpenAlexW2297945512

What OpenQuestion holds

Textmetadata
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.